The interaction of environmental mutagens with animal cells and cells from human body fluids will be studied using antinucleoside antibodies. With fixed cells the antibodies react only with DNA which has undergone strand breaks or is denatured. Normally, only cells in S are immunoreactive, they can be scored using immunofluorescence or immunoperoxidase methods. Immunoreactivity can be induced in normally unreactive G1 cells by X-irradiation or by treatment with drugs such as camptothecin which are known to induce DNA strande breaks. Drugs such as cytosin arabinoside, hydroxyurea, and Actinomycin D (0.04 micrograms per ml) are not active. Cycloheximide and other protein synthesis inhibitors induce (reversible) immunoreactivity in Gl HeLa cells. Our preliminary studies showed that mutagens such as N-acetoxy-acetylaminofuorescence (10 mcg/ml) and N-methyl-N'nitro-N-nitrosoguanidine (4 mcg/ml) induced intense nuclear fluorescence in 90% of Gl HeLa cells. These chemicals are know to induce DNA strand breaks. They are others such as polycyclic hydrocarbons, form covalent links with nucleic acids. Immunoreactivity may signal this interaction. Further study is needed to examine the interaction of these and other mutagens to determine if this technique can be useful in identifying their action on animal cells. Flow microfluorometry increase the efficiency of this novel approach to the study of chemical carcinogens. Recent unpublished studies showed that high doses of diagnostic ultrasound also induce immunoreactivity in Gl HeLa cells. This deserves urgent study, in view of the above and the now routine exposure of developing human fetus to this modality. Using known chemical carcinogens as models we will correlate immunoreactivity protein synthesis inhibition, and covalent attachment of radiolabeled carcinogens RNA and DNA.